SPN is a rare neoplasm with low malignant potential. Surgical resection is warranted even in the presence of local invasion or metastases as patients demonstrate excellent long-term survival. Positive immunoreactivity for Ki-67 may predict the malignant potential and poor outcome of SPNs.

BackgroundWe summarize our experience of the diagnosis, surgical treatment, and prognosis of solid pseudopapillary tumors (SPTs).MethodsWe carried out a retrospective study of clinical data from a series of 17 patients with SPT managed in two hospitals between October 2001 and November 2011.ResultsAll of the 17 patients were female and the average age at diagnosis was 26.6 years (range 11 years to 55 years). The tumor was located in the body or tail in ten patients, the head in five patients, and the neck in two patients. The median tumor size was 5.5 cm (range 2 cm to 10 cm). All 17 patients had curative resections, including seven distal pancreatectomies, five local resections, four pancreaticoduodenectomies, and one central pancreatectomy. Two patients required concomitant splenic vein resection due to local tumor invasion. All patients were alive and disease-free at a median follow-up of 48.2 months (range 2 to 90 months). There were no significant associations between clinicopathologic factors and malignant potential of SPT. Ki-67 was detected in three patients with pancreatic parenchyma invasion.ConclusionsThe SPT is an infrequent tumor, typically affecting young women without notable symptoms. Surgical resection is justified even in the presence of local invasion or metastases, as patients demonstrate excellent long-term survival. Positive immunoreactivity for Ki-67 may predict the malignant potential of SPTs.

A growing body of evidence confirms that long non-coding RNAs (lncRNAs) have an important role in biological processes by regulating gene expression at multiple levels. Dysregulated lncRNAs may be potential prognostic biomarkers or targets for the development of cancer treatments. However, the prognostic role of an lncRNA signature in pancreatic cancer has not been investigated. Pancreatic cancer lncRNA expression profiles from The Cancer Genome Atlas (TCGA) were analyzed in the current study. The prognostic value of differentially expressed lncRNAs (DElncRNAs) was evaluated via the Kaplan-Meier method. A risk score model was established based on the potential prognostic lncRNAs. The biological functions of lncRNAs were predicted by functional enrichment analysis. Then, an lncRNA-mRNA co-expression network was established and predicted the function of the lncRNAs. Seven DElncRNAs that were significantly associated with the prognosis of pancreatic cancer were identified. Patients were classified into high-risk and low-risk groups using a risk score based on a three-lncRNA signature. There was a significant difference in overall survival (OS) between the groups (median OS 1.33 vs. 3.65 years; log-rank test, P=0.0000). Cox regression analysis and ROC curves demonstrated that the three-lncRNA signature may be an effective independent prognostic biomarker in patients with pancreatic. The functional enrichment analysis showed that lncRNA AL137789.1, one component of the three-lncRNA signature, may be associated with tumor immune responses. In the present study, a novel three-lncRNA signature that was established that may be useful in predicting survival among patients with pancreatic cancer. These lncRNAs may be involved in tumor immunity and thus affect the prognosis of patients.

Abstract. Yes-associated protein (YAP) serves an essential role in tumorigenesis. However, the potential role and the molecular mechanism underlying the effect of YAP on hepatocellular carcinoma (HCC) cells have not been elucidated. In the current study, it was revealed that YAP expression was increased significantly in HCC cancer tissues and its overexpression was associated with tumor differentiation. The silencing of YAP by small interferring RNA led to the inhibition of HCC cell growth, which was associated with the promotion of apoptosis. The silencing of YAP also decreased the invasive potential of HCC cells and the activity of the phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase (AKT) signaling pathway. Furthermore, silencing of YAP increased the chemosensitivity of HCC cells to cisplatin (CDDP) through inactivation of the PI3K/AKT signaling pathway. In vivo studies using PDTX model suggested a promotive role for YAP in the growth of HCC and knockdown of YAP increased the anti-tumor activity of CDDP. Taken together, these results revealed that YAP is overexpressed in HCC, and promotes proliferation, invasion and drug resistance of HCC cells. Inhibition of YAP, alone or in combination with traditional chemotherapy, may effectively combat HCC.

Our data suggested that it is a potential approach to increasing the number of intraepithelial attacking CD8+T cells for tumor immunotherapy, and exploring a new mechanism for immunosuppression in a tumor microenvironment with high T cell infiltration without attack.